CNS tumours and ICP Flashcards
In which region of the cranium do childhood tumors arise?
How would it present?
Posterior fossa
Enlarged head and hydrocephalus in children
In which region of the cranium do adult tumors arise?
Cerebral hemispheres- supratentorial
Discuss the local spread of CNS tumors.
May infiltrate the dura, skull, sinuses
Tumours are able to spread through the CSF implantation along the brain and spinal cord at a distance from the original tumour site (seeding)
Discuss meningiomas.
Benign
Usually dura
from meningothelial cells of the arachnoid
Gross:
Rounded masses with well-defined
Dural bases that compress the underlying brain
Extension into the overlying bone may be present
Discuss the Astrocytomas:Pilocytic astrocytomas (grade I).
Common childhood
cerebellum, but also the floor of walls of the third ventricle, optic nerves, and occasionally cerebral hemisphere
Often cystic with a mural nodule
Discuss the Astrocytomas: Diffuse astrocytoma (grade 2)
young adults mid-30s
Tumour is poorly defined, gray, infiltrative, expands and distorts the invaded brain
Firm or soft and gelatinous; cystic degeneration may be seen
Discuss the Astrocytomas: Anaplastic astrocytoma (grade 3).
4th decade
cortex and white matter, frontal lobe
Typically invade the surrounding brain without overt tissue destruction
Mass-like appearance on cut section
Discuss the Astrocytomas: Glioblastoma (grade 4).
Frequent in adults
cerebral hemispheres
High grade
die in 6 months
Poorly defined mass with necrosis and haemorrhage
Discuss Oligodendrogliomas (grade 2)
4th and 5th decades
cerebral hemispheres and prediction for white matter.
Well-circumscribed, gelatinous, gray masses
Often with cysts, focal hemorrhage, and calcification
Discuss Ependymomas (grade 2).
arise next to the ependyma-lined ventricular system and central canal of the spinal cord.
Occurs in children and adults
May seed along the CSF pathway down the spinal cord
Slow-growing tumors and the prognosis is usually good
Well-demarcated, solid or papillary mass arising from the floor of the ventricle
Discuss medulloblastoma.
Children-cerebellum
aggressive
local infiltration
sensitive to radiotherapy
Discuss Choroid plexus tumours.
Papillomas and carcinomas
papillary and intraventricular.
hydrocephalus and seeding via the CSF pathway
Discuss Primary lymphomas of the brain.
immunosuppressed, AIDS
high grade
Diffusely infiltrative
From which site can tumours metastasize to the brain?
Most common primary sites are:
Lung
Breast
Skin (melanoma)
Kidney
Gastrointestinal tract
RARE: choriocarcinoma, but has a high likelihood of metastasizing to the brain
How does cranial pressure usually increase?
generalized cerebral oedema
increased CSF volume (hydrocephalus)
Focally expanding mass lesions
Outline the clinical features of the increased ICP.
Oedema of the optic papilla (papilloedema) with blurred vision
Nausea and vomiting due to pressure on the pons and medulla (vomiting centre)
Headache due to distension of the dura
Neck stiffness due to pressure around the cerebellar cones
Impaired consciousness
Ininfants: macrocephaly, bulging fontanelle, sunset sign
Increased pressure gradient within theskullin the presence of inflexible brain structures (e.g.Tentorium cerebelli) → flexible brain tissueshifts→ possiblebrain tissueherniation
Cushing triad: ): irregular breathing, elevated systolic BPandbradycardia
Discuss the Cushing triad.
(if brainstem is compressed): irregular breathing, elevated systolic BPandbradycardia
↑ Intracranialpressure→↓ perfusionpressure within the brain → compensatory activation of thesympathetic nervous systemto maintain cerebral perfusion →↑systolicblood pressure→ stimulation ofaortic archbaroreceptors→ activation of theparasympathetic nervous system(vagus) →bradycardia
↑ Pressureonbrainstem→dysfunction ofrespiratory center→ irregular breathing
Outline the pathways of oedema formation in the brain.
Vasogenic oedema: increase in extracellular fluid due to increased vascular permeability.
Cytotoxic oedema: increase in intracellular fluid (cell swelling) secondary to neuronal, glial, or endothelial cell membrane injury
Interstitial oedema (hydrocephalic oedema) occurs when an increase in intravascular pressure causes an abnormal flow of fluid from the intraventricular CSF across the ependymal lining to the periventricular white matter.
Describe the gross appearance cerebral oedema.
Gyri are flattened and widened
Intervening sulci are narrowed
Ventricular cavities are compressed
What are the causes of hydrocephalus?
Obstructive: obstruction to CSF outflow - commonest
Excess production: seen with choroid plexus tumours
Decreased reabsorption: Rare
Describe the effect of hydrocephalus in infants.
An increased volume of CSF within the ventricles expands them and can increase the intracranial pressure.
When hydrocephalus develops in infancy before closure of the cranial sutures, there is enlargement of the head increased head circumference (macrocephaly)
Hydrocephalus developing after this period is associated with expansion of the ventricles and increased intracranial pressure, without a change in head circumference
Define non-communicating hydrocephalus.
obstructive hydrocephalus: ventricular system is obstructed and does not communicate with the subarachnoid space, as may occur because of a mass in the third ventricle
Define communicating hydrocephalus.
the ventricular system is in communication with the subarachnoid space, and there is enlargement of the entire ventricular system.
Define Hydrocephalus ex vacuo.
compensatory increase in ventricular volume secondary to a loss of brain parenchyma.
Define cerebral herniation.
Displacement of brain tissue past rigid dural folds (the falx and tentorium) or through openings in the skull because of increased intracranial pressure.
Discuss subfalcine herniation.
cingulate gyrusof one hemisphere is compressed and herniates under thefalx cerebri→compression of:
Contralateralhemisphere→ obstruction of theforamen of Monro→hydrocephalus
Pericallosal arteries→hemiparesis(predominantly lower limbs)
Discuss uncal herniation.
medialtemporal lobe(the uncus) herniates at the tentorial incisure
→Compression of:
Ipsilateraloculomotor nerve palsy→fixed and dilated pupil
Ipsilateralposterior cerebral artery→cortical blindnesswithcontralateralhomonymous hemianopia
Contralateralcerebral peduncle →ipsilateralparalysis +Kernohan’s phenomenon(a syndrome ofuncal herniationcharacterized by pupillary dilationipsilateralto theherniation, due toCN IIIcompression) and, paradoxically,ipsilateralweakness (due tocontralateralcerebral peduncle compression). This is unusual because commonly, anipsilateralbrain lesion results incontralateralmotor symptoms. It occurs in patients withincreased ICPcaused by intracranial hemorrhage orcerebral edema.)
→Downward shift of thebrainstem→brainstemhemorrhages → focal deficits, impaired consciousness, death
Discuss foramen magnum herniation.
structures of theposteriorfossa (e.g.,cerebellar tonsils, medulla) herniate at theforamen magnum→ impaired consciousness, decerebrate posturing,apnea, impaired circulation, death
What is the medical therapy for Increased ICP?
Osmotic diuretics
IVmannitol: can generally be administered every6–8 hours, effects last for up to24 hours
IV hypertonicsaline: particularly forshort-termtreatment
Removal ofCSFvia an intraventricular monitor with drainage system (e.g., external ventricular drain) or acerebral shunt(e.g., inhydrocephaluspatients)
Describe the pathogenesis of papilloedema.
Vasogenic oedema involves more severely the white matter and extends along the optic nerves and into the optic papillae (papilloedema)
The oedematous optic papillae protrude forward into the vitreous chamber and displace the retina, causing blurring of vision
Fundoscopic examination reveals blurred disk margins
Define sunset signs.
Pressure on CN 3,4,6
forces eyes down
revealing a rim of sclera
